It is known from, for example, in the EP-A-0 970 713 and its corresponding U.S. Pat. No. 6,574,507 B1, commonly assigned herewith to ELA Medical S.A. Montrouge, France, to diagnose and treat respiratory disorders such as the apnea revealing a pathology known as “sleep apnea syndrome” (SAS). In a general manner, this SAS respiratory pathology is characterized by the frequent occurrence of apnea during a phase of sleep of the patient (e.g., at least 10 to 20 events per hour). An “apnea” (also known as a respiratory pause) is defined as a temporary cessation (or stop) of the respiratory function of a duration that is greater than approximately 10 seconds. The SAS pathology also can be characterized by the occurrence of hypopnea under the same frequency conditions. A “hypopnea” is defined as a significant decrease (but without interruption) of the respiratory flow, typically a decrease of more than 50% as compared to a previously acquired respiratory flow reference.
The interruption or the reduction of the respiratory flow involves a reduction in the oxygen concentration of blood (also known as the oxygen saturation), and the occurrence of unconscious, micro waking-up events. This pathology, which is found in more than 50% of those patients patients suffering from a cardiac insufficiency condition, has as a consequence inter alia a diurnal somnolence, a loss of attention, an increase in the risks of road (automobile) accidents, and a higher incidence of hypertension.
The above mentioned EP-A-0 970 713 and U.S. Pat. No. 6,574,507 B1 discloses apparatus and methods for diagnosing the occurrence of an apnea from a minute-ventilation signal (“signal VE,” also designated as “signal Mv”), which is a parameter of physiological preponderance generally obtained by a measurement of intrathoracic impedance. The signal MV provides a continuous indication of the respiration rate and the respiratory flow volume of the patient. If an apnea occurs during a phase (also called a “state”) of sleep of the patient (the sleep state of the patient can be, for example, indicated by an activity sensor of physical preponderance such as an accelerometer), then the device delivers a cardiac stimulation at a frequency that is slightly higher than the natural sinusal rate/rhythm of the patient. This increased frequency is provided to increase the blood flow in order to be able to reduce the incidence of the oxygen desaturation caused by a SAS.
The starting point of this invention lies in the observation by the inventors that a systematic increase of the heart rate in response to a detection of apnea or hypopnea is not always a suitable treatment. Indeed, it has been reported that for certain patients the apnea or hypopnea could be followed by an adrenergic reaction. Such a reaction naturally induces a light tachycardia and a significant increase in blood pressure, sufficient to compensate for the fall of the ventilatory activity. Among these patients, the myocardium thus can react naturally by adapting its contractility so as to increase the blood flow. In this way, the myocardium maintains the blood appreciably at the same level of oxygen saturation.
Ideally, to decide whether or not it is necessary to apply to the myocardium a stimulation at a frequency higher than the natural sinusal rate/rhythm of the patient, the best criterion would be a direct measurement of oxygen saturation in blood. Then, the stimulation would be started only in the event of a proven and significant desaturation. But such a direct measurement of oxygen saturation is difficult to implement in a simple and permanent manner in the context of an active implanted medical device, given the current state of the art.